Abstract

Purpose

The aim of this work is to investigate the roles of solute carrier family 22 member 18 (SLC22A18) in lipid metabolism and in establishing the tumor phenotype of HepG2 cells.

Methods

SLC22A18-knockdown HepG2 cells were established by stable transfection with shRNA. Protein expression levels were measured by quantitative proteomics and Western blot analysis. Cell growth was examined by cell counting kit. Accumulation of triglyceride-rich lipid droplets was measured by Oil-Red O staining. Cell migration and invasion were examined by Transwell assays.

Notes

ACKNOWLEDGMENTS AND DISCLOSURES

We are grateful for partial financial support through three Grants-in-Aid for Scientific Research from the Japanese Society for the Promotion of Science (JSPS) for Research Activity Start-up (No. 24890170), Young Scientific Research (B) (No. 26860109) and Scientific Research (C) (No. 16 K08373), as well as a grant from the Takeda Science Foundation. S. Ohtsuki is a full professor at Kumamoto University and is also a director of Proteomedix Frontiers. This study was not supported by the company, and its position at the company did not influence the design of the study, the collection of the data, the analysis or interpretation of the data, the decision to submit the manuscript for publication, or the writing of the manuscript and did not present any financial conflicts. The other authors declare no competing interests.

Authorship Contributions

S. Ito, G. Honda. and S. Ohtsuki contributed to the study design. S. Ito, G.Honda, Y. Fujino, S. Ogata, M. Hirayama-kurogi and S.Ohtsuki conducted experiments and performed data analysis. S. Ito and S. Ohtsuki wrote the manuscript. All authors gave final approval for the manuscript to be published.

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